Hypokalemia
Adult-Gerontology Acute Care Practice Guidelines
Definition
A.Serum potassium concentration of less than 3.5 mEq/L (see Box 5.3).
Incidence
A.Hypokalemia occurs in 20% of hospitalized patients.
Pathogenesis
A.Causes.
1.Total body deficiency (increased losses or decreased intake). This condition may develop as a result of:
a.Gastrointestinal losses.
b.Renal losses with or without metabolic abnormalities.
c.Decreases in intake that surpass the kidneys’ ability to compensate.
2.Redistribution (a net shift of potassium from extracellular to intracellular space).
3.Hypomagnesemia. This causes the kidneys to secrete potassium into the urine at a higher rate than they would with the same potassium levels and higher magnesium levels, leading to hypokalemia or accelerating it.
4.Elevated plasma sodium levels (due to a high salt diet). These cause the kidneys to lose potassium while making an effort to balance ion neutrality via available ion exchange transporter.
Predisposing Factors
A.Nonpotassium sparing diuretics.
B.Eating disorders.
C.Alcoholism.
Subjective Data
A.Common complaints/symptoms.
1.Palpitations or arrhythmias.
2.Gastrointestinal.
a.Nausea and vomiting.
b.Constipation, ileus.
3.Muscle weakness (severe hypokalemia).
a.Skeletal muscle weakness and paralysis.
b.Respiratory compromise due to diaphragmatic paralysis.
c.Rarely, rhabdomyolysis.
4.Cramping (lower legs).
B.Postural hypotension.
Physical Examination
A.EKG changes include ST-segment depression, T-wave flattening, T-wave inversion, and the presence of U-waves.
B.Can progress to life-threatening and/or fatal arrhythmias and sudden cardiac death.
1.Check gastrointestinal system: Abdominal pain and bowel sounds.
2.Inspect musculoskeletal system: Strength.
3.Perform neurological examination.
Diagnostic Tests
A.Initial lab tests.
1.Serum potassium (preferably plasma).
2.Venous or arterial CO2 or HCO3 and/or pH.
B.Other lab tests.
1.Complete chemistry panel.
2.Blood urea nitrogen (BUN) and creatinine to assess kidney function.
C.Estimate of total body extracellular potassium and potassium deficit.
1.Total body potassium (mEq/L) = Extracellular fluid volume (ECFV) × Serum potassium (mEq/L).
a.ECFV = Total body water [0.6 × weight (kg)] × 1/3.
2.Potassium deficit (mEq/L) =
a.ECFV × Desired serum potassium (4.0 or 4.5 mEq/L) – ECFV × Serum potassium (mEq/L).
b.NOTE: This calculation does not account for ongoing losses or intracellular deficits.
D.Assessment for cause of potassium losses.
1.Trans-tubular potassium gradient (TTKG): Assessment of the kidney’s capability to appropriately conserve potassium.
a.Valid only if the patient is not taking any diuretics or drugs to block the renin–angiotensin–aldosterone system (RAAS).
b.During hypokalemia, TTKG should be less than 3, indicating the kidneys are conserving potassium.
2.Urine potassium concentration—24-hour collection.
E.Cardiac function.
1.EKG changes including peaked T-waves, prolonged PR-interval, widened QRS complex, shortened QT-interval.
2.Bradyarrhythmias.
3.Ventricular fibrillation.
4.Asystole.
Differential Diagnosis
A.Spurious hypokalemia or pseudohypokalemia.
1.Leukocytosis greater than 100,000/mm³.
2.Insulin dosing/timing of lab draw.
B.Redistribution.
1.Metabolic alkalosis.
2.Catecholamine excess.
a.Alkalemia.
b.Familial hypokalemic periodic paralysis.
c.Thyrotoxicosis.
d.Factor replacement in megaloblastic anemia.
e.Medications: Insulin, theophylline toxicity, β– adrenergic activity/agents (epinephrine), bronchodilators, caffeine-containing drugs.
C.Increased potassium losses.
1.Gastrointestinal losses: Prolonged vomiting or diarrhea.
2.Extra-renal potassium loss (urine potassium < 20 mEq/24 hours).
a.Prolonged diarrhea.
b.Nasogastric suctioning.
c.Intestinal potassium binders (e.g., sodium polystyrene sulfonate or patiromer).
d.Poor intake/malnutrition.
e.Laxative abuse.
f.Excessive sweating.
g.Villous adenoma recto-sigmoid colon.
3.Renal potassium loss (urine potassium >20 mEq/24 hours): Non anion gap metabolic acidosis.
a.Renal tubular acidosis Type I (distal) and Type II (proximal).
b.Liddle’s syndrome (decreased aldosterone secretion; normal renin level).
c.Diabetic ketoacidosis, lactic acidosis.
d.Ureterosigmoidostomy.
e.Medications: Carbonic anhydrase inhibitors, laxative overuse, topiramate.
4.Renal potassium loss (urine potassium >20 mEq/24 hours): Metabolic alkalosis.
a.Vomiting or nasogastric suction.
b.Mineralocorticoid excess syndromes (normotensive primary hyperaldosteronism).
c.Bartter’s syndrome.
d.Gitelman’s syndrome.
e.Medications: Diuretics (loop, thiazide), especially in the setting of high salt intake.
5.Renal potassium loss (urine potassium >20 mEq/24 hours): No acid–base disorder.
a.Elevated renin levels: Malignant hypertension, renovascular disease, renin-secreting tumor.
b.Low renin levels: Elevated aldosterone levels (primary hyperaldosteronism, bilateral adrenal hyperplasia, dexamethasone suppression).
c.Low aldosterone levels.
i.Mineralocorticoid ingestion.
ii.Congenital adrenal hyperplasia.
iii.Cushing’s syndrome.
iv.Ectopic ACTH.
v.Tobacco.
vi.Black licorice.
d.Hypomagnesemia.
e.Enuresis/polyuria: Hypercalcemia, acute kidney injury recovery, postobstructive diuresis, osmotic diuresis (e.g., hyperglycemia).
f.Medications: Aminoglycosides, amphotericin B, high dose corticosteroids, mineralocorticoids.
6.Other.
a.Leukemia.
b.Any disorder causing severe or progressive weakness: Myasthenia gravis, polyneuropathy.
Evaluation and Management Plan
A.Goal: To avoid or resolve the cause of the hypokalemia and treat the condition and its related symptoms.
B.Step 1—Immediate treatment: Potassium supplementation. The total dose is at least equal to the calculated potassium deficit. The calculated dose to replace potassium in extracellular fluid is:
1.[Ideal plasma potassium mmol/L − Actual plasma potassium] × [TBW (L) × Extracellular fluid (%)].
a.TBW = Weight (kg) × 0.5 (women), 0.6 (men), 0.45 (elderly).
b.ECFV is 26% to 30% of TBW.
2.[4.0 mmol/L–2.5] × [(80 kg × 0.5) × 0.26] = 1.5 × [40 x 0.26] = 1.5 × 10.4 = 15.6 mmol/L or 16.
a.16 mmol/L–16 mEq/L
b.Deliver intravenously. Oral doses will be higher due to poor absorption.
C.Step 2—Repeated calculations and doses for ongoing potassium losses.
1.Intravenous supplementation.
a.Initial dose of 20 to −40 mEq: Common, but in severe hypokalemia will likely need to be repeated.
b.Dose: 10 to 20 mEq/hr.
c.Reserved for severe and/or symptomatic hypokalemia or for patients unable to tolerate oral supplementation.
2.Oral supplementation.
a.Available in tablet, capsule, or liquid formulations.
b.Total daily doses: 40 to 100 mEq; sufficient replacement in most cases.
c.Divided into two to four doses to reduce gastrointestinal side effects.
d.Patients with renal dysfunction: Decrease dose by 50% and avoid repeating doses.
D.Step 3—Treatment of underlying disorder.
1.Correct hypomagnesemia as it can result in refractory hypokalemia.
2.Decrease or discontinue medications associated with hypokalemia if possible.
3.Decrease sodium intake (especially with diuretic use).
E.Step 4—Treatment of other electrolyte and acid–base disorders.
F.Step 5—Assessment of need for chronic management.
1.Some patients will require chronic oral potassium supplements or high potassium diets.
2.Consider potassium-sparing diuretics (e.g., spironolactone, amiloride, triamterene) in patients on potassium-depleting medications.
3.All patients on potassium-depleting medications need a low-salt diet.
Follow-Up
A.For hypokalemia related to acute episodes, such as severe diarrhea, no follow-up is necessary.
B.However, patients on long-term diuretic therapy should have periodic monitoring of serum potassium levels.
Consultation/Referral
A.Consult nephrology for any refractory electrolyte disorder with or without acute kidney injury or chronic kidney disease (CKD).
B.Consult endocrinology for any uncontrolled diabetes or other hormone disorders.
C.Consult gastroenterology for refractory symptoms and suspected villous adenoma.
Special/Geriatric Considerations
A.Monitor patients with CKD, congestive heart failure, or medications associated with hypokalemia carefully to avoid overcorrecting.
Bibliography
Allon, M. (2014). Disorders of potassium metabolism. In D. S. Gipson, M. A. Perazella, & M. Tonelli (Eds.), National Kidney Foundation’s primer on kidney diseases (6th ed., pp. 90–99). Philadelphia, PA: Elsevier Saunders.
Cohnm, J. N., Kowey, P. R., Whelton, P. K., & Prisant, L. M. (2000). New guidelines for potassium replacement in clinical practice. Archives of Internal Medicine, 160, 2429–2436. doi:10.1001/archinte.160.16.2429
Kraft, M. D., Btaiche, I. F., Sacks, G. S., & Kudsk, K. A. (2005, August). Treatment of electrolyte disorders in adult patients in the intensive care unit. American Journal of Health System Pharmacy, 62(16), 1663–1682. doi:10.2146/ajhp040300
Pepin, J., & Shields, C. (2012). Advances in diagnosis and management of hypokalemic and hyperkalemic emergencies. Emergency Medical Practice, 14(2), 1–20.